Download Representation of the Visual Field in the Human Occipital Cortex

CLINICAL SCIENCES
Representation of the Visual Field
in the Human Occipital Cortex
A Magnetic Resonance Imaging and Perimetric Correlation
Agnes M. F. Wong, MD; James A. Sharpe, MD
Objectives: To evaluate the retinotopic map of the human occipital cortex by correlating magnetic resonance
imaging (MRI) findings with visual field defects in patients with occipital lobe infarcts and to assess the compatibility between our cliniconeuroimaging findings and
the location of lesions predicted by the classic Holmes
map and a revised map.
Methods: Magnetic resonance images were obtained in
14 patients with occipital lobe infarcts. Visual field analysis was performed with tangent screen, the Goldmann
perimeter, and the Humphrey Field Analyzer. Based on
the pattern of visual field deficit, the location of the lesion in the mesial occipital lobe in each patient was predicted using the Holmes map and other retinotopic maps
of the occipital cortex. The predicted location of the lesion was then compared with its actual location shown
on MRI to assess the compatibility between our data and
the other maps. These maps determine retinotopic cor-
M
From the Division of Neurology
and the Department of
Ophthalmology, The Toronto
Hospital and the University of
Toronto, Toronto, Ontario.
relates of the medial occipital lobe, but they cannot establish correlates of the striate cortex (V1). The medial
occipital representation of central vision was evaluated
by regression analysis.
Results: The MRI correlations in this study confirmed
gross estimates of the retinotopic organization of the occipital cortex. However, our findings did not correlate
exactly with the Holmes map. We determined that the
central 15o of vision occupies 37% of the total surface area
of the human medial occipital lobe. Based on our data, a
refined retinotopic map is presented.
Conclusions: The resolution of conventional MRI testifies to its considerable value in localizing occipital lobe
lesions. Our findings support, and refine, the Holmes map
of the human occipital cortex.
Arch Ophthalmol. 1999;117:208-217
our knowledge of the representation of the visual
field in the human occipital cortex was derived from studies of patients with penetrating injuries to the head during
wartime. Inouye,1 Holmes and Lister,2 Holmes,3,4 and, later, Spalding5 correlated visual field deficits with the location of missile wounds in the occiput and produced
retinotopic maps of the striate cortex.
The map presented by Holmes4 is
widely adopted as a detailed representation of the visual field in the human striate cortex. It depicts a point-to-point localization of the contralateral hemifield of
vision in the striate cortex. The upper field
is represented in the inferior calcarine cortex, and the lower field is represented in
the superior cortex. The central field occupies the posterior pole, whereas the peripheral field is mapped anteriorly.4 The
macula, which subserves central vision, has
a disproportionately large cortical repreUCH OF
ARCH OPHTHALMOL/VOL 117, FEB 1999
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sentation4—up to 25% of the surface area
of the striate cortex has been assigned to
the central 15° of vision.6
The accuracy of the Holmes map was
later supported by activation study of the
visual cortex using positron emission tomography scanning7 and by cliniconeuroimaging correlation using computed tomography (CT).8-11 Spector et al,11 using
CT to study patients with occipital lobe infarction, reported a good match between
cliniconeuroimaging findings and the location of lesions predicted by the Holmes
map. However, these studies were limited by the resolution of early CT scans.
With the introduction of magnetic resonance imaging (MRI), Horton and Hoyt6
reexamined the Holmes map. By correlating MRI findings with homonymous field
deficits in 3 patients with occipital lobe lesions, they found that the Holmes map did
not correlate well with their findings.
Based on their findings, together with
electrophysiologic data on Old World primates—which showed that in macaque
PATIENTS AND METHODS
Consecutive patients with visual field defects and occipital lobe lesions seen in the neuro-ophthalmology clinic at
The Toronto Hospital, Toronto, Ontario, were screened using the central 30-2 threshold program of the Humphrey
Field Analyzer (Allergan-Humphrey Instruments, San Leandro, Calif). Patients with incomplete homonymous hemianopia were included in the study. The central 30-2 program only tests the retinal threshold at 76 predetermined
points within the central 30° of vision, with 19 points tested
in each quadrant. For example, adjacent to the horizontal
meridian, the tested points lie at approximately 2°, 8°, 14°,
20°, and 26° of eccentricity. Thus, the program does not
provide information on the retinal threshold at approximately 3° to 7°, 9° to 13°, 15° to 19°, 21° to 25°, and 27° to
30° of eccentricity, although the gray-scale printout gives
the impression that the threshold at every point is tested.
In this study, all recruited patients were also tested with
tangent screen and Goldmann perimetry to delineate more
precisely the extent of visual field loss. If there was discrepancy among the 3 perimetric measurements, the mean
value of the 3 measurements was used (in all study patients, the discrepancy among measurements was #5°).
Serial axial and sagittal T 1 -weighted (repetition
time = 516-517 milliseconds and echo time = 8-11 milliseconds) and T2-weighted (repetition time = 2200-4383 milliseconds and echo time = 80-95 milliseconds, 2 separate
acquisitions) images with a slice thickness of 5 mm were
obtained in all recruited patients using the 1.5-T Signa imaging system, version 5.4.2 (General Electric Medical Systems, Milwaukee, Wis). The MR images were then processed on a workstation (SUN/SPARC 10 “Advantage
Windows,” General Electric Medical Systems). Patients with
well-defined infarcts in the occipital cortex with a minimum duration of 3 months were included in the study. Patients with lesions that may have functional neurons remaining within the neuroimaged boundaries, such as edema
or hemorrhage secondary to tumors, arteriovenous malformations, or primary intracerebral hemorrhages, were excluded. Using a software program (Advantage Window v.1.2,
General Electric Medical Systems), the anterior and posterior extent of the infarct (as measured by its linear distance from the occipital pole) was independently determined by assessing T1- and T2-weighted images in axial
(along the calcarine fissure) and midsagittal orientations
by us. If there were discrepancies in measurements between T1 vs T2 images, orientations, or between us, the mean
distance from the occipital pole was used (in all study patients, the discrepancy between measurements was #3 mm).
Using the same software program, the infarcted and nor-
monkeys as much as 70% of the total surface area of the
striate cortex is occupied by the central 15° of vision12,13—
Horton and Hoyt6 proposed that the cortical magnification of the human striate cortex is scaled to that in the
macaque striate cortex. They concluded that the Holmes map underestimated the cortical magnification of central vision, and they proposed a revised map.6 In that revised map,6 the human striate cortex was approximately
an ellipse measuring about 80 3 40 mm. The area subserving central vision was expanded such that approxi-
mal portions of the occipital cortex were traced out using
a pointing device independently by us, and the corresponding surface areas were calculated by the planimetric program available in the software. If there was a discrepancy
in measurements between us, the mean surface area was
used (in all study patients, the discrepancy between measurements was #30 mm2).
To assess the accuracy of the Holmes map4 and a revised map,6 the location of the lesion in each patient was
predicted using the 2 maps based on the patient’s visual
field defect. We then compared the predicted location of
the lesion with its actual location on MRI to assess the compatibility between our data and the 2 maps.
To evaluate the cortical representation of central vision, the percentage of the surface area of the infarcted or
noninfarcted (see below) occipital cortex was plotted against
the degree of eccentricity from fixation.
In patients with posterior lesions that began at the occipital pole, the surface area of the lesions was used in the
analysis. For example, patient 1 (Figure 1), who had an
inferior scotoma extending from 2° to 10°, was shown to
have an infarct extending from the occipital pole to 12 mm
anteriorly above the calcarine fissure by MRI, which measured 300 mm2. Assuming the total surface area of the average human striate cortex to be about 2500 mm2 (based
on postmortem specimens and after allowing for shrinkage),6,14 the percentage of surface area of the lesion above
the calcarine fissure was calculated to be 12%, which corresponded to an eccentricity of 10°. Because the area above
and below the calcarine fissure is represented at any eccentricity, 24% (12% 3 2) of the total surface area was assigned to an eccentricity of 10°.
In patients with anterior lesions that began at some
distance from the occipital pole, the surface area of the normal area of the occipital cortex posterior to the lesions was
used. For example, patient 4 (Figure 2), who had an inferior quadrantanopia sparing the central 11°, was shown
to have a lesion that began at 16 mm and extended anteriorly to 25 mm from the occipital pole above the calcarine fissure. The surface area of the normal cortex posterior to the lesion above the calcarine fissure was 375 mm2,
representing 15% of the total surface area and corresponding to an eccentricity of 11°. Therefore, 30% (15% 3 2) of
the total surface area was assigned to an eccentricity of 11°.
Regression analysis of the relationship between eccentricity from fixation and the corresponding percentage
surface area of the medial occipital cortex was performed.
The percentage of the area of the occipital cortex subserving the central 15° of vision was then determined. Based
on the cliniconeuroimaging findings in study patients, we
constructed a new retinotopic map of the human occipital
cortex.
mately 70% of the total surface area of the human striate
cortex was assigned to the central 15° of vision.
We correlated MRI findings with the location and
extent of visual field deficits in a series of patients with
occipital lobe infarcts to determine the retinotopic representation of the human occipital cortex. To assess the
accuracy of the Holmes map4 and a revised map,6 we compared our cliniconeuroimaging findings with the locations of lesions predicted by the 2 maps. Based on the
findings in our patients, the percentage of the total sur-
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3/1000W
A
3/1000W
A
No FC
No FC
LE
RE
LE
B
RE
B
I2e
I2e
I2e
I1e
I3e
I1e
I4e
I2e
I4e
I3e
I4e
I4e
C
C
Figure 1. Patient 1. A, Right homonymous paracentral scotoma in the lower
quadrant shown by tangent screen. B, Mapping of the scotoma using
Goldmann perimetry revealing the scotoma to be dense to V4e object and to
extend from 2° to 10°. C, Axial T2-weighted magnetic resonance image
showing a lesion beginning at the tip (white arrowhead) of the left occipital
pole and extending anteriorly for 12 mm (black arrowhead). FC indicates
finger counting; W, white test object.
Figure 2. Patient 4. A, Left homonymous inferior quadrantanopia shown by
tangent screen. B, Mapping by Goldmann perimetry revealing sparing of
central 11°, without sparing of the temporal crescent. C, Sagittal magnetic
resonance image showing a lesion beginning at 16 mm and extending
anteriorly to 25 mm from the right occipital pole (black arrowheads).
FC indicates finger counting; W, white test object.
face area of the medial occipital cortex devoted to central vision was estimated, and a refined retinotopic map
is presented.
tangent screen, and Goldmann perimetry. Figure 4 shows
the visual field defects on tangent screen, and a schematic representation of the location of the corresponding lesions, using the axial brain templates by Damasio
and Damasio.15
The visual field defect, the locations of the lesions
predicted by the Holmes4 map and a revised map6 based
on visual field loss, and the actual locations of the lesions on MRI scans are shown in Table 2. For example, for patient 1, who has a right homonymous inferior quadrant scotoma from 2° to 10°, the Holmes map
predicts a lesion to extend from the occipital pole to
9 mm anteriorly, whereas a revised map6 predicts it to
RESULTS
Fourteen patients had well-defined infarcts in the occipital cortex on MRI scans and were included in the
analysis (Table 1). There were 9 males and 5 females,
with ages ranging from 17 to 74 years (mean, 50 years).
The mean duration of lesions was 14 months (range, 3-84
months). All 14 patients had incomplete homonymous
visual field defects by Humphrey perimetry (Figure 3),
ARCH OPHTHALMOL/VOL 117, FEB 1999
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Table 1. Patient Characteristics*
Patient No./
Sex/Age, y
Side of
Lesion
Lesion Location
on MRI, mm†
Duration of
Lesion, mo
Visual Field Findings
1/M/37
2/F/71
3/M/48
4/F/45
5/F/21
6/F/28
7/M/80
8/M/52
9/M/65
10/M/17
11/M/65
12/M/64
13/M/74
14/F/68
Left
Right
Right
Right
Left
Left
Left
Right
Right
Left
Left
Right
Right
Right
0-12
0-18
0-22
16-25
4-23
8-34
11-24
10-40
0-5
7-31
2-40
0-2
0-4
9-35
14
5
4
8
84
3
8
3
10
25
16
3
3
5
Right homonymous inferior quadrant scotoma 2°-10°
Left homonymous hemianopic scotoma 0°-12°
Left homonymous inferior quadrantanopia sparing central 2°
Left homonymous inferior quadrantanopia sparing central 11°
Right homonymous hemianopia sparing central 5°
Right homonymous superior quadrantanopia sparing central 5°
Right homonymous inferior quadrantanopia sparing central 9°
Left homonymous inferior quadrantanopia sparing central 8°
Left homonymous inferior quadrant scotoma 0°-6°
Right homonymous hemianopia sparing central 5°
Right homonymous superior quadrantanopia sparing central 2°
Left homonymous inferior quadrant scotoma 0°-2°
Left homonymous inferior quadrant scotoma 0°-6°
Left homonymous inferior quadrant scotoma sparing central 6°
*MRI indicates magnetic resonance imaging.
†Distance from the occipital pole.
Patient 1
Patient 6
Patient 11
Patient 2
Patient 7
Patient 12
NLP
Patient 3
Patient 8
Patient 13
Patient 4
Patient 9
Patient 14
Patient 5
Patient 10
Figure 3. Visual field defects on Humphrey automated perimetry of the 14 study patients. NLP indicates no light perception.
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3/1000W
Patient 1
No FC
3/1000W
Patient 2
No FC
3/1000W
Patient 3
No HM
HM
No HM
3/1000W
Patient 4
No FC
3/1000W
Patient 5
HM
No HM
Patient 6
3/1000W
3/1000W
Patient 7
HM
Figure 4. Axial brain templates showing the occipital lesions of the 14 patients with their corresponding visual field defects on tangent screen.
FC indicates finger counting; HM, hand movement; W, white test object; and NLP, no light perception.
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3/1000W
Patient 8
No FC
3/1000W
Patient 9
No FM
HM
Patient 10
3/1000W
HM
Patient 11
3/1000W
3/1000W
Patient 12
FC
NLP
3/1000W
Patient 13
FC
3/1000W
Patient 14
HM
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Table 2. Visual Field Defects, Predicted Locations of the Lesions Based on the Holmes Map4 and a Revised Map,6 and the Actual
Locations of the Lesions on MRIs*
Predicted Lesion Location†
Patient
No.
Visual Field Findings
Holmes Map
Revised Map
1
2
3
4
5
6
7
8
9
10
11
12
13
14
Right homonymous inferior quadrant scotoma 2°-10°
Left homonymous hemianopic scotoma 0°-12°
Left homonymous inferior quadrantanopia sparing central 2°
Left homonymous inferior quadrantanopia sparing central 11°
Right homonymous hemianopia sparing central 5°
Right homonymous superior quadrantanopia sparing central 5°
Right homonymous inferior quadrantanopia sparing central 9°
Left homonymous inferior quadrantanopia sparing central 8°
Left homonymous inferior quadrant scotoma 0°-6°
Right homonymous hemianopia sparing central 5°
Right homonymous superior quadrantanopia sparing central 2°
Left homonymous inferior quadrant scotoma 0°-2°
Left homonymous inferior quadrant scotoma 0°-6°
Left homonymous inferior quadrant scotoma sparing central 6°
0-9 mm
0-13 mm
1 mm-end
10 mm-end
3 mm-end
3 mm-end
8 mm-end
7 mm-end
0-5 mm
3 mm-end
1 mm-end
0-1 mm
0-5 mm
5-25 mm
8-32 mm
0-37 mm
8 mm-end
34 mm-end
22 mm-end
22 mm-end
31 mm-end
30 mm-end
0-23 mm
22 mm-end
8 mm-end
0-8 mm
0-23 mm
23 to .50 mm
Location of Lesion
on MRI, mm†
0-12
0-18
0-22
16-25
4-23
8-34
11-24
10-40
0-5
7-31
2-40
0-2
0-4
9-35
*MRI indicates magnetic resonance imaging; end, the juncture of the parieto-occipital and calcarine fissures.
†Distance from occipital pole.
extend from 8 mm from the occipital pole to 32 mm anteriorly. However, on MRI, the actual location of the lesion began at the occipital pole and extended to 12 mm
anteriorly, which was in close agreement with the predicted location according to the Holmes4 map. Similarly, for patient 14, who has a left homonymous inferior quadrant scotoma sparing the central 6° (Figure 5,
A and B), the Holmes map predicts a lesion to begin at 5
mm from the occipital pole and to extend rostrally to 25
mm from the pole; on the other hand, a revised map6 predicts it to begin at 23 mm from the occipital pole and to
extend beyond 50 mm from the pole. However, on MRI
(Figure 5, C), the actual lesion began at 9 mm from the
occipital pole and extended to 35 mm from the pole, a
finding that was in close agreement with the predicted
location according to the Holmes4 map. For the remaining 12 patients (Table 2), the locations of lesions predicted by the Holmes map were in closer agreement with
their actual locations on MR images than were those predicted by a revised map.6
A plot of the percentage of the surface area of the
infarcted or noninfarcted occipital cortex vs eccentricity from fixation is shown in Figure 6. The best-fit linear regression is represented by the solid line; 37% of the
total surface area of the medial occipital cortex subserves the central 15° of vision.
COMMENT
Our correlations of MRI findings with visual field
defects in patients with occipital lobe lesions confirmed
gross estimates of the retinotopic organization of the
occipital cortex. However, the visual field deficits in our
patients did not correspond exactly to the Holmes
map,4 and they did not correlate with a revised map,6
which was based on findings in 3 other reported
patients. In addition, we found that 37% of the total
surface area of the medial occipital cortex subserves the
central 15° of vision.
From the visual field and imaging findings in our
patients, a refined retinotopic map is presented
(Figure 7). Figure 7 illustrates that the human occipital cortex is situated along the superior and inferior lips
of the calcarine fissure. The foveal representation is located posteriorly at the occipital pole, whereas the peripheral visual field is represented anteriorly at the juncture of the parieto-occipital and calcarine fissures. Because
the extent of striate cortex (V1) is not determined by imaging, the retinotopic correlation is with MRI of the medial occipital cortex, not with the retinotopic organization of area V1.
Several limitations confound conventional MRI in
correlating lesion location with visual field defects. These
limitations also apply to CT imaging of occipital lesions.8-11 First, because visual processing in the striate cortex is organized in ocular dominance columns that have
a cross-sectional width of 0.4 mm,16 5-mm cuts that are
widely used in major MRI centers may not provide sufficient resolution to determine the exact extent and location of the lesion identified by perimetry. However, because the rostral-caudal extent of lesions in our 14 patients
differed more than 5 mm from a revised map,6 which was
based on MR images of 3 patients whose slice thickness
was not specified,6 limitation of slice thickness does not
explain the disparate result. Second, the determination
of the extent of the lesion is complicated by areas of edema
surrounding the lesion, which may be difficult to differentiate from the actual area of infarction. However, all
our patients were imaged many months or years (mean
duration of lesions, 14 months) after the onset of visual
field loss, when edema should have completely resolved. Third, tissue damage may disrupt function but
be undetected by imaging. For example, patients 3 through
7 and 10 had homonymous field defects without sparing of the temporal crescent, indicating that the most anterior portion of the occipital pole should be involved.
However, on MRI, no signal change was detected in the
anterior medial occipital cortex, suggesting that tissue
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Surface Area of the Occipital Cortex, %
3/1000W
A
60
50
40
30
20
10
0
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
Eccentricity, Degrees
HM
LE
Figure 6. Percentage of the surface area of the infarcted or noninfarcted
occipital cortex vs eccentricity from fixation. The solid line represents the
best-fit regression line of the values from 14 patients.
RE
B
I3e
I4e
I3e
I4e
V4e
V4e
C
1 cm
Figure 7. Proposed retinotopic map of the occipital cortex as viewed from
the mesial surface of the occipital lobe with the calcarine fissure opened.
Numbers, in degrees, and the corresponding dashed lines represent visual
field eccentricity along meridians. The dashed line in the calcarine fissure
represents the horizontal meridian. The dashed lines at the border of the
occipital cortex represent eccentricities along the lower (upper dashed line)
and upper (lower dashed line) vertical meridians.
Figure 5. Patient 14. A, Left homonymous inferior quadrant scotoma with
sparing of the central 6° shown by tangent screen. B, Goldmann perimetry
showing the scotoma to be dense to V4e object. C, Sagittal magnetic
resonance image showing a lesion beginning at 9 mm and extending
anteriorly to 35 mm from the right occipital pole (black arrowheads).
HM indicates hand movemet; W, white test object.
damage may extend beyond visible MRI change; alternatively, the monocular temporal crescent of field (representing the nasal retina of the contralateral eye) may
not extend to the extreme anterior part of the occipital
cortex, although this seems unlikely. Fourth, areas of signal change in MRI do not specify destruction of all neural elements, which may be spared in an area of visible
damage. This pertains particularly to neoplasms and hemorrhages, which we therefore excluded from our study.
Fifth, because we used a 2-dimensional image to estimate the size of a 3-dimensional lesion, the accuracy of
measurements depends on the orientation of the cuts.
However, there is no ideal head orientation for studying
the calcarine fissure because the incline of the calcarine
fissure relative to other brain and skull reference coordinates is variably oriented among individuals,17 and it
also varies with minor changes in head position. Finally, and most important, the exact boundaries of the
striate cortex cannot be determined by MR images, and
there is a natural and substantial variation across individuals in the exact dimension and location of the striate cortex.14 Moreover, no compensation for cortical infolding or curvature of the calcarine fissure can be made
using MR images, which allows only estimation of the
extent of the lesion.
The discrepancy between the results of the present
study and those leading to a revised map6 may be due in
part to the small number of patients on whom a revised
map was based (3 patients). In addition, whereas we excluded lesions that may have functional neurons remaining within the neuroimaged boundary, a revised map6 included 2 patients with such lesions (1 patient had a
tuberculoma and another had an arteriovenous malformation), which may lead to an overestimation of the ac-
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tual area of damage. Although that revised map6 was later
supported by McFadzean and coworkers18 using either
CT or MRI in a larger series of patients, they also included 11 patients with such lesions (neoplasms, arteriovenous malformations, cerebromalacia, and hematomas). Moreover, because edema and an ischemic
penumbra frequently surround the area of infarction, we
only included MR images that were performed at least 3
months after patients’ initial presentation, when they
should have resolved. However, because previous MRI
studies6,18 did not specify the duration of lesions in their
patients, bordering ischemia and edema may partly explain the disparate results.
Based on endogenous changes in magnetic susceptibility caused by localized activity-dependent variations in blood flow and oxygenation, functional MRI
(fMRI) has been used to map human cortical activity during stimulation of selected areas of the visual field in normal subjects.19-21 Sereno et al21 and Engel et al,22 using
fMRI, found that there is emphasis on the center of gaze
in the human primary visual cortex. However, their results are not consistent with our data and those from previous studies.7-11 Potential sources of spatial spread, such
as that caused by lateral neural connections within the
cortex and experimental artifacts (eg, slight head movement and brain pulsatility),22 may limit the spatial resolution of fMRI to accurately determine cortical magnification. Moreover, these studies measured a traveling wave
of activity in the cortex of normal subjects by slowly
changing the position of the stimuli pattern. Although
these subjects were instructed to fixate at the center of
the stimuli display, no attempts were made to monitor
eye position during testing. Even the smallest eye movement can affect the measurement, especially at the exact
center of the fovea. In addition, fMRI detects changes in
signal from venous blood, not the activity of neural tissue. Some investigators23 suggested that much of the signal change seen in fMRI might be seen within brain areas having little or no neural tissue, being instead images
of the venous vasculature.
Correlation of visual field defects with neuropathologic change at autopsy may further clarify the topographic representation of the visual field in the human
striate cortex.24,25 After flattening the complete striate
cortex in 4 normal adult patients with 1 eye and reconstructing the ocular dominance columns mosaic, Horton and Hocking26 identified the blind spot representation, which lacks ocular dominance columns and
extends from 12° to 18° along the horizontal meridian.
They reported that 42% to 62% (mean ± SD, 52% ± 2%)
of the human striate cortex corresponds to the central
12° of vision. Horton and Hoyt6 presumed that human
striate cortex and that of macaque monkeys had about
the same cortical magnification of the central visual
field, being 70% for the central 15°.12,13 However, Horton and Hocking26 reported that the cortical magnification of the central 12° of vision was 60% in monkeys
and 42% to 62% (mean, 52%) in humans, an area less
than that estimated in a revised map6 and considerably
smaller than that estimated by fMRI.21 Flattening procedures26 are subject to distortions that could affect
retinotopic data. Three-dimensional MRI reconstruc-
tion of slices in different orientations may better correlate anatomy with visual field loss. Although the
boundaries of striate cortex are not defined by neuroimaging methods, imaging correlates of lesions with
visual field defects provide in vivo information about
the retinotopic representation of vision in the occipital
lobe.
The primary aim of this study was to establish a
direct link between the anatomy of the medial occipital
cortex along the calcarine fissure and the visual field
locus and the extent of functional deficit. However,
there is a limited causal relationship between the individual vagaries of the calcarine anatomic features and
the retinotopic characteristics of a visual field defect. A
more accurate and direct relationship is more likely to
be between the location of cortical neurons receiving
input from restricted receptive field positions in the
retina and the location of a lesion with respect to those
neurons. The arrangement of cortical neurons with
respect to the gross anatomy of the calcarine fissure can
be quite variable. Fundamentally, then, anatomically
based retinotopic maps proposed by Holmes, 4 others,1,5,6 and us are limited in their accuracy. However,
the location of lesions within the medial occipital cortex on imaging studies has substantial value in determining whether the pattern of a patient’s visual field
defect is adequately accounted for by imaging. Establishing the validity of the existing retinotopic maps
based on lesion data therefore becomes important to
account for the symptoms of occipital cortex lesions.
Our MRI correlations confirmed estimates of the retinotopic organization of the medial occipital cortex and
corresponded better with the Holmes4 map than with a
revised map6 based on conventional MRI correlations of
lesions in 3 other reported patients. Thirty-seven percent of the total surface area of the mesial surface of the
human occipital cortex subserves the central 15° of vision. Although precise knowledge of the retinotopic representation of the human striate cortex (V1) is limited
by imaging techniques, the resolution of MRI testifies to
its considerable value in diagnosing and localizing occipital lobe lesions.
Accepted for publication September 22, 1998.
This study was supported by grant MT 5404 from the
Medical Research Council of Canada.
We thank David Mikulis, MD, for his expert advice.
Reprints: James A. Sharpe, MD, Division of Neurology, The Toronto Hospital, EC 5-042, 399 Bathurst St,
Toronto, Ontario, Canada M5T 2S8.
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3. Holmes G. Disturbances of vision by cerebral lesions. Br J Ophthalmol. 1918;2:
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4. Holmes G. The organization of the visual cortex in man. Proc R Soc Lond B Biol
Sci. 1945;132:348-361.
5. Spalding JMD. Wounds of the visual pathway, II: the striate cortex. J Neurol Neurosurg Psychiatry. 1952;15:169-183.
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ARCHIVES Web Quiz
B
e sure to visit the Archives of Ophthalmology’s World Wide Web site (http://www.ama-assn.org/ophth) and try your
hand at our new Clinical Challenge interactive quiz. We invite visitors to make a diagnosis based on selected
information from a case report or other feature scheduled to be published in the following month’s print edition of
the ARCHIVES. The first visitor to e-mail our Web editors with the first correct answer wins an Archives of Ophthalmology
CD-ROM and will be recognized in the print journal and on our Web site. A full discussion of the case featured in the quiz
can be found in the following month’s print edition of the journal.
ARCHIVES Web Quiz Winner for December 1998:
Our congratulations to the winner of our Clinical Challenge, Iman Ezzat Ahmed Abu-elenein, MOphth, Alexandria, Egypt.
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